Blood Glucose Regulation
Glucose maintained at 80-100mg/100 ml between meals. Enters cells by facilitated diffusion, converted
to glucose-6-phosphate, cannot recross plasma membrane. This continues through glycolysis to produce
ATP. If excess, forms glycogen.
If excess, stored as glycogen or fat
Glycogenesis > converts excess glucose to glycogen, most in skeletal muscle and liver.
When glycogen stores are full, glucose and amino acids synthesize lipids (LIPOGENESIS). Glucose
molecules form glyceraldehyde-3-phosphate and acetyl-CoA. Amino acids can be converted to Acetyl-
CoA too. Glyceraldehyde-3-phosphate is converted to glycerol, 2-carbon acetyl-CoA molecules join to
form fatty acid chains. Glycerol and 3 fatty acids combine to form triglycerides *.
Glucose is needed > glycogen is broken down to glucose-6-phosphate through GLYCOGENOLYSIS. In
skeletal muscle, glucose-6-phosphate goes through glycolysis to produce ATP. Liver uses it for energy or
converts it to glucose which is released into blood. Skeletal muscle lacks enzymes to convert glucose-6-
phosphate to glucose, CANT release glucose into blood.
Glucose releases from liver to maintain blood glucose levels between meals. When liver glycogen levels
are inadequate to supply glucose, its synthesized from proteins or lipids (GLUCONEOGENESIS). Amino
acids can be converted into citric acid cycle molecules (acetyl-CoA or pyruvic acid) then to glucose.
Glycerol is converted to glyceraldehyde-3-phosphate then to glucose.
Lipids are 99% of body’s energy storage, glycogen is 1%.
Stored as triglycerides in adipose tissue. Synthesis/breakdown of triglycerides occur constantly, between
meals they are broken down and fatty acids are released into blood (Free fatty acids). Skeletal
muscle/liver use these for energy source.
Adipose Lipase> breaks triglycerides into fatty acids/glycerol
Beta Oxidation > metabolism of fatty acids, reactions where 2 C atoms are removed at the end of fatty
acid chains to form Acetyl-CoA. Continues to remove them until entire fatty acid chain is converted to
Acetyl-CoA molecules. Can enter citric acid cycle and be used to make ATP.
Ketogenesis > acetyl-CoA can be used here, formation of ketone bodies. When a lot of Acetyl-CoA
produced in liver, 2 acetyl-CoA molecules combine to form ACETOACETIC ACID, then converted to B-
hydroxybutyric acid and acetone. These are all KETONE BODIES., released into blood, go to other tissues,
converted back into acetyl-CoA (in tissues) then go to citric acid cycle to produce ATP. Ketosis > excessive production of ketone bodies, when they exceed capacity of body’s buffering system,
a decrease in blood pH (acidosis) occurs.
Starvation, low carb diets, diabetes mellitus can increase rate of ketone body formation.
Ketone bodies excreted by kidneys and diffuse into lung alveoli. Diabetes mellitus > ketone bodies in
urine and acetone breath.*
Amino acids taken up by cells (liver),